Marine biomedicine is an important field in oceanology and bio-ecosystem and has evolved significantly alongside advances in biotechnology and growing understanding of marine life. In this perspective, we propose a refined concept of clinical marine biomedicine, with a clear mission to establish an emerging discipline that bridges marine biomedicine and clinical practice. The exploration of marine-origin sources should be emphasised, with a strong focus on the identification, validation and development of human disease-specific diagnostics and target-oriented pharmaceutics. The perspective headlines some of critical components, including marine-oriented human evolution and development, humanised marine-based models, biomarker innovation and validation, marine microbiomes and metabolites, and target nutrition and therapy. We envision that clinical marine biomedicine will become a crucial pillar clinical molecular medicine, contributing to the improvement of human health and the prognosis of patient.
Objective: This study aims to systematically investigate the potential harms of Large Language Models (LLMs) in the peer review process.
Background: LLMs are increasingly used in academic processes, including peer review. While they can address challenges like reviewer scarcity and review efficiency, concerns about fairness, transparency and potential biases in LLM-generated reviews have not been thoroughly investigated.
Methods: Claude 2.0 was used to generate peer review reports, rejection recommendations, citation requests and refutations for 20 original, unmodified cancer biology manuscripts obtained from eLife's new publishing model. Artificial intelligence (AI) detection tools (zeroGPT and GPTzero) assessed whether the reviews were identifiable as LLM-generated.All LLM-generated outputs were evaluated for reasonableness by two expert on a five-point Likert scale.
Results: LLM-generated reviews were somewhat consistent with human reviews but lacked depth, especially in detailed critique. The model proved highly proficient at generating convincing rejection comments and could create plausible citation requests, including requests for unrelated references. AI detectors struggled to identify LLM-generated reviews, with 82.8% of responses classified as human-written by GPTzero.
Conclusions: LLMs can be readily misused to undermine the peer review process by generating biased, manipulative, and difficult-to-detect content, posing a significant threat to academic integrity. Guidelines and detection tools are needed to ensure LLMs enhance rather than harm the peer review process.
Background: Sitosterolemia is a rare, inherited, autosomal recessive disorder of lipid metabolism. Patients with sitosterolemia may exhibit diverse, distinct clinical characteristics.
Methods and results: We report cases of sitosterolemia with haematological abnormalities as primary initial symptoms. Both patients were seen with symptoms of haemolytic anaemia and thrombocytopenia. Their plasma levels of low-density lipoprotein-cholesterol were normal. Genetic tests were arranged as stomatocytes were found in their peripheral blood smears. Three heterozygous mutations in adenosine triphosphate-binding cassette subfamily G member 5 (ABCG5) were identified in case 1. A mutation in integrin beta 3 was discovered in case 2, while no mutations were found in ABCG5 or ABCG8. Sitosterolemia was considered for both cases, and Ezetimibe was used for treatment, with quick curative responses.
Conclusion: For patients with unexplained haemolytic anaemia, thrombocytopenia, especially with stomatocytes present in peripheral blood, the diagnosis of sitosterolemia should be considered, and genetic testing is recommended.
Background: Elevated platelet count is correlated with poor survival of lung cancer. Platelet factor 4 (PF4), a platelet-specific protein, plays an important role in platelet function. Emerging evidence suggests that regulation of PF4 can modulate platelet function to impact the progression of lung cancer.
Methods: Anti-PF4 antibody was used to neutralise PF4 to regulate platelet function in the co-culture of platelets and lung cancer cells lines of H1299 and A549. The proliferation, apoptosis and cell cycle were examined by cell counting kit-8 (CCK-8) test and flow cytometry.
Results: Anti-PF4 antibody inhibited the proliferation of H1299 and A549 cells when stimulated with platelets, yet induced cell cycle arrest and cell apoptosis only in A549, not H1299. The proliferation, cell cycle distribution and apoptosis were not affected by anti-PF4 antibody in A549TP53‒ cells.
Conclusion: Anti-PF4 antibody exerted anti-proliferative effects by inducing apoptosis and cell cycle arrest in lung cancer cells without TP53 mutation via p53 signalling pathway when stimulated with platelets.
Phosphatidylethanolamine (PE) is a pivotal glycerophospholipid that constitutes a significant portion of cellular membranes, playing a crucial role in maintaining membrane fluidity, supporting protein integration, and mediating signal transduction. In the lungs, PE is also a key component of pulmonary surfactant, which is essential for preserving alveolar stability and facilitating efficient gas exchange. Recent research has highlighted the association between dysregulated PE metabolism and various lung diseases, such as asthma, pulmonary fibrosis and chronic obstructive pulmonary disease. Nevertheless, the molecular mechanisms underlying these associations remain poorly understood, and the potential of PE as a therapeutic target or biomarker for lung diseases has yet to be fully explored. This review aims to provide a comprehensive overview of the biological functions and biosynthetic pathways of PE, with a particular focus on its roles in pulmonary physiology and pathology. We summarise current findings on PE alterations in different lung diseases and discuss the potential implications of targeting PE metabolism for therapeutic interventions.
Background: Neoadjuvant chemotherapy combined with immunotherapy (NACI) has shown promise in oesophageal squamous cell carcinoma (ESCC). However, a significant proportion of patients exhibit resistance to NACI, and the underlying mechanisms remain unresolved.
Methods: We integrated single-cell RNA sequencing data, including seven patients with ESCC treated with NACI and 69 patients with ESCC treated with surgery alone. Bulk RNA sequencing data were obtained from a public database. Immunohistochemistry and multiplexed immunofluorescence staining were performed to verify the role of important immune cells and molecules in clinical treatment outcomes.
Results: Here, we profiled the transcriptomes of 512 736 cells from 76 patients with ESCC, revealing that the nonresponder baseline tumour microenvironment exhibited a relative absence of major histocompatibility complex II molecules expressed on CD20+B cells and a low expression of CXCL13 on CD4_Tfh and CD8_Tex cells. We also identified CD68+CD163+ macrophages that highly expressed the immunosuppressive LGALS9 gene and preferentially accumulated in the nonresponders after NACI treatment. In addition, nonresponders had a higher baseline fraction of POSTN+fibroblasts, which is associated with higher infiltration of CD68+CD163+ macrophages and lower infiltration of germinal centre B cells. Finally, we described the different characteristics of malignant epithelial cells from different pathological responses to tumours.
Conclusions: This study has unveiled a potential regulatory network among immune cells, stromal cells and malignant epithelial cells under different pathological response conditions and provides a valuable resource for discovering novel targeted therapies for ESCC.